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CELLULAR PATHOLOGY > mechanisms of oncogenesis > Flashcards

mechanisms of oncogenesis Flashcards

1
Q

what are some lifestyle factors that are linked to cancer

A

smoking

obesity and weight

hormones

alcohol

sun and UV

lack of physical activity

poor diet

inherited genes

air pollution

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2
Q

Why is cancer defined as a disease of aging?

A

The older you get, the higher the risk of developing cancer

The longer we live the more time there is for DNA to accumulate mutations that may lead to cancer

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3
Q

What is cancer?

A

Disease of the loss of control of cell signalling pathway

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4
Q

Cancer is a group of diseases characterised by 4 distinct hallmarks. What are they?

A
  • Abnormal cell proliferation
  • Tumour formation
  • Invasion of neighbouring normal tissue
  • Metastasis to form new tumours at distant sites
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5
Q

What are carcinomas?

A

Cancers that occur in the epithelial cells

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6
Q

What are sarcomas?

A

Cancers that occur in the mesoderm cells (muscle and bone)

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7
Q

What are adenocarcinomas?

A

Cancers that occur in the glandular tissue

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8
Q

what are the 10 hallmarks of cancer

A
  • evading growth suppressors
  • avoiding immune destruction
  • enabling replicative immortality
  • tumour promoting inflammation
  • activating invasion and metastasis
  • inducing angiogenesis
  • genome instability and mutation
  • resisting cell death
  • deregulating cellular energetics
  • sustained proliferative signaling
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9
Q

what is meant by hallmarks of cancer

A

all the characteristics a normal cell has to undergo to become a tumour cell

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10
Q

what effect do carcinogens have on DNA

A

Carcinogens cause alterations to the DNA - mutation

DNA from tumours has been shown to contain many alterations from point mutations to deletions.

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11
Q

how does accumulation of DNA mutations occur and what does it result in

A

This accumulation occurs only after the cells defense mechanism of DNA repair have been evaded

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12
Q

what is germline mutation

A

Alteration in DNA (point mutations/deletion) within an egg or sperm cell is known as a germline mutation

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13
Q

can germline mutations be passed onto offspring

A

These mutations can be passed onto your offspring (it is an inheritable mutation)

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14
Q

how do germline mutations affect the risk of developing cancer

A

This does increase your risk of developing cancer BUT does not necessarily mean you will develop cancer immediately

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15
Q

how is germline mutation different to somatic mutation

A

germline mutation:
inheritable mutation

somatic mutation:
Cannot be passed on, found in daughter cells during cell division but it is NOT inheritable

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16
Q

describe the process of tumour formation from a single somatic cell

A

alteration in DNA of somatic cell

All cells in a primary tumour arise from a single cell: initiation of the
development of cancer is clonal

cell division of mutated cell = production of clonal cells = tumour formation

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17
Q

what do tumours that arise from somatic mutations do to help themselves survive

what is meant by sub clonal mutations?

A

It is the continued accumulation of mutations within the tumour (the tumour will continue to evolve and accumulate changes to help themselves survive)

clones that has arised from the same transformed cell but that have accumulated different mutations in them to help the tumour survive (this also explains the heterogeneity of cells in a tumour). this also explains why cells from the same tumour respond differently to treatment.

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18
Q

normal cells can receive signals to stimulate proliferation. What are 3 examples of these signals/

A
  • growth factors (PDGF, EGF)
  • cytokines (growth hormone, IL)
  • hormones (oestrogen)
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19
Q

in terms of proliferation and apoptosis, what is the balance between these in healthy cells?

A

proliferation = cell loss

HEALTHY CELLS

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20
Q

how do tumours arise from a normal cell

A

there are many genes involved in the regulation of the growth, apoptosis and differentiation of cell numbers

mutation in the genes that regulate these processes can lead to an imbalance between proliferation and cell loss

uncontrolled cell proliferation = tumour formation

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21
Q

what are the 2 categories of genes that regulate cell growth

A

oncogenes

tumour suppressor genes

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22
Q

what is the difference between oncogenes and proto-oncogenes

A

a proto oncogene codes for proteins responsible for cell proliferation

proto oncogene –> activated oncogene via mutation = leads to signals that cause uncontrolled growth
(tumour formation = cancer)

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23
Q

Role of tumour suppressor genes

A

Tumour suppressor genes inhibit both growth and tumour formation

They act as breaking signals during G1 phase of the cell cycle, to stop or slow the cell cycle before S phase (before DNA replication)

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24
Q

what happens if there is a mutation in the tumour suppressor gene

A

If tumour-suppressor genes are mutated, the normal brake mechanism will be disabled, resulting in uncontrolled growth (progression of cell cycle = tumor formation = cancer)

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25
the formation of a tumour occurs as a result of changes to which 2 genes and what changes occur
This means the formation of a tumour as a result of: 1. mutation in proto-oncogene ---> activated oncogene 2. mutation in tumour suppressor gene
26
What are the 3 assumptions made for carcinogenesis models?
1. Malignant transformation of a single cell is sufficient to give rise to a tumour 2. Any cells in a tissue are equally likely to be transformed 3. Once a malignant cell is generated the mean time to tumour detection is generally constant
27
What are the 5 models of cancer?
Model 1: mutational (genotoxic) Model 2: genome instability  Model 3: non-genotoxic  Model 4: Darwinian (evolving tumour) Model 5: tissue organisation
28
what are the 4 carcinogens categories
chemical physical heritable (predisposition) viral
29
examples of chemical carcinogens
polycyclic aromatic hydrocarbons aromatic amines nitrosamines alkylating agents
30
examples of physical carcinogens
radiation such as ionising and UV
31
examples of viral carcinogens
hepatitis B Epstein Barr
32
What are the 4 major groups that exert their carcinogenic effects by adding functional groups to DNA bases called DNA adducts?
1. Polycyclic aromatic hydrocarbons 2. Aromatic amines 3. Nitrosamines 4. Alkylating agents
33
What is found in coal tar and how is this related to cancer?
Coal tar contains benzo(a)pyrene. It enters cells VERY easily and when activated can become carcinogenic
34
describe benzo(a)pyrene and how it is related to cancer | where is it commonly found - how does it get into our bodies?
Benzo(a)pyrene (BP) is a procarcinogen (NOT CARCINOGENIC) When BP is taken into our bodies (via cigarette smoke) and is acted upon by microsomal enzymes, it is converted into Benzo(a)pyrene epoxide via addition of functional group. This is when it becomes carcinogenic.
35
What effect does Benzo(a)pyrene epoxide have on DNA?
IT IS A CARCINOGEN | Changes G----> T in DNA
36
What test can be carried out to find out if something is carcinogenic?
Ames Test A test to determine the mutagenic activity of chemicals by observing whether they cause mutations in sample bacteria mutation in bacteria = chemical is carcinogenic
37
how does the Ames test work
You take rat liver extract (contains the microsomal enzymes), you mush it up and you combine it with a Salmonella strain that will only grow in the presence of histidine.  If you plate that onto an agar plate that lacks histidine, following overnight incubation, you should have very few colonies on that plate. (If you get one or two, it’s due to natural reversion) If you add the carcinogen being tested, and then plate it, and then you get lots of colonies, it suggest that there is now a change in the bacteria, and it can now grow in the absence of histidine. This confirms that the compound you’re testing is in fact carcinogenic.
38
How do physical carcinogens act?
Unlike chemical carcinogens physical carcinogens act by imparting energy into the biological material
39
Physical carcinogens include radiation. What 2 types can act as carcinogens?
ionising radiation (x-ray, nuclear radiation) UV radiation
40
How does radiation act on DNA? Is this reversible?
Radiation is a physical carcinogen Radiation damages DNA by causing DNA breaks or pyrimidine dimers These damages can be repaired BUT if not this leads to failed repair which leads to translocations and mutations
41
Describe heritable carcinogens and the relation to cancer
An inherited germline mutation has an increased risk of developing certain tumours but are RARELY involved in CAUSING cancer immediately
42
in hereditary malignant syndromes, what is the elevated cancer risk due to
In most hereditary malignant syndromes, the elevated cancer risk is due to a mutation of a single gene (monogenic hereditary diseases)
43
How could heritable carcinogens lead to an increase risk of cancer
most cases = mutation of a single gene The affected genes usually have a controlling function on the cell cycle, apoptosis or the repair of DNA damage A deficiency in DNA repair would cause more DNA damages to accumulate, and increase the risk for cancer (predisposition for cancer)
44
What are germline mutations? | can it be inherited
Present in egg or sperm Can be inherited Cause cancer family syndrome
45
what are the 2 groups of syndrome predisposing to cancer
DNA repair defects chromosomal abnormalities
46
examples of DNA repair defects predisposing to cancer
* Ataxia telangiectasia * Bloom's syndrome * Fanconi's anaemia * Li-Fraumeni syndrome * Lynch type II * Xeroderma pigmentosum
47
examples of chromosomal abnormalities predisposing to cancer
* Down's syndrome | * Klinefelter's syndrome
48
What is Ataxia telangiectasia ('spider veins')? mutation in what gene?
* Neuromotor dysfunction * Dilation of blood vessels * Mutation in ATM gene
49
what is the ATM gene
Codes for serine/threonine kinase (its function is to phosphorylate P53) that is recruited and activated by dsDNA breaks leading to cell cycle arrest, DNA repair and apoptosis
50
ATM gene codes for serine/threonine kinase. | What is the function of serine/threonine kinase
its function is to phosphorylate P53
51
what can mutation in the ATM
mutation in gene = improper function in DNA repair etc
52
What is Ataxia telangiectasia ('spider veins') a cancer predisposition for
Lymphoma Leukaemia Breast cancer
53
blooms syndrome what do people with this look like? (in terms of height) what happens in this syndrome?
short stature (rarely exceed 5ft) skin rash that develops after skin exposure
54
what happens in Bloom syndrome
mutation of BLM gene
55
what is the function of the BLM gene
Provides instructions for coding a member of the RecQ helicase family that help maintain the structure and integrity of DNA
56
what is Bloom syndrome a cancer predisposition for
Basal cell carcinoma Squamous cell carcinoma
57
What is Lynch type II?
Mutation in DNA mismatch repair genes (MMR genes): MLH1 MSH2 MSH6 PMS2
58
what is Lynch type II a cancer predisposition for
colorectal cancer
59
sign of Lynch type II
NO SYMPTOMS First sign that a person has Lynch type II is when symptoms of bowel and womb cancer develops
60
Describe viruses as carcinogens
Most harm is caused when viruses multiply inside the infected cell, kill the cell (lysis) and release progeny to further infect other cells In rare incidences it switches to a latent cycle BUT Some viruses can be tumorigenic (allow transformation of cells; tumour formation)
61
What are some properties required of tumorigenic viruses? (3)
stable association with cells must not kill cells must evade immune surveillance of infected cells
62
how do tumorigenic viruses form a stable association with cells
- chromosomal integration  | - episome (can replicate independently of chromosomal DNA)
63
how do tumorigenic viruses ensure they do not kill host cells
- non-permissive host (virus cannot replicate)  - suppression of viral lytic cycle  - viral release by budding 
64
how do tumorigenic viruses evade immune surveillance
- immune suppression  | - viral antigens not expressed at cell surface
65
List some viruses that are associated with human cancer and the type of cancer they can result in 1. DNA VIRUSES 2. RNA VIRUSES
DNA VIRUSES 1. Epstein-Barr virus • Burkitt's lymphoma • Nasopharyngeal carcinoma 2. Papilloma virus • Cervical carcinoma • Warts 3. Hepatitis B and C • Hepatoma RNA RETROVIRUSES  • HTLV-I (Adult T-cell leukaemia, lymphoma)
66
What is retinoblastoma?
A childhood cancer that affects the retina
67
What causes retinoblastoma?
RB1 (the tumour suppressor gene) causes retinoblastoma when BOTH COPIES are mutated
68
DESCRIBE Knudson's hypothesis for hereditary cancers
Knudson found that there were 2 sets of patients: 1. Patients presenting with the tumour at an early age 2. Patients presenting with the tumour at a later age He then found out this was because there are 2 types of retinoblastoma: 1. The inherited form (as a result of a mutation in the Rb gene) 2. The sporadic form in the inherited form, the patients would have acquired the second mutations (and therefore both) at a much earlier age than the sporadic (non inherited) form. In the sporadic forms of the tumour both mutations had to take place and hence this could explain the difference of age at diagnosis.  Stage at which they would have acquired BOTH mutations and therefore retinoblastoma? inherited = earlier in life sporadic = later in life
69
describe the non genotoxic model of cancer
Non-genotoxic carcinogens have been shown to act as:  - tumour promoters   - endocrine-modifiers - receptor-mediators   - immunosuppressants - inducers of tissue-specific toxicity and inflammatory responses
70
example of non genotoxic carcinogen that acts as tumour promoters
1,4-dichlorobenzene
71
example of non genotoxic carcinogen that acts as endocrine modifiers
17β-estradiol
72
example of non genotoxic carcinogen that acts as receptor mediators
2,3,7,8-tetrachlorodibenzo-p-dioxin
73
example of non genotoxic carcinogen that acts as immunosuppressants
cyclosporine
74
example of non genotoxic carcinogen that acts as inducers of tissue-specific toxicity and inflammatory responses
metals such as arsenic and beryllium
75
describe the darwinian model of carcinogens
1. carcinogen exposure = normal cell accumulates mutations 2. Natural selection This mutated cell will undergo changes to form a tumour (transformation) 3. Tumour cells will be selected for ability to grow and invade (This tumour cell will also undergo artificial selection: when treating a patient with chemotherapy some tumour cells become resistant to the treatment = these tumour cells will therefore be able to expand and grow) There can be the ODD mutation that is a disadvantage to the tumour cell (rare)
76
Describe model 5: tissue organisation Two drastically different approaches to understanding the forces driving carcinogenesis have crystallized through years of research What are they?
1. Somatic mutation theory (SMT) | 2. Tissue organisation field theory (TOFT)
77
Describe the somatic mutation theory (SMT)
Cancer is derived from a single somatic cell that has successively accumulated multiple DNA mutations. Those mutations damage the genes which control cell proliferation and the cell cycle.  If these changes are not repaired = carcinogenesis
78
Describe the tissue organization field theory (TOFT)
Carcinogenic agents destroy the normal tissue architecture, thus disrupting cell-to-cell signalling and compromising genomic integrity.  The DNA mutations are random and the effect of the tissue disruption, not the cause
79
What is the immune system's response to cancer? does this get rid of the cancer?
The immune system will: - protect from virus-induced tumours  - eliminate pathogens  - identify and eliminate tumour cells  This leads to immune surveillance. However, despite this, tumours can still arise. 
80
What is cancer immunoediting?
ELIMINATION:  The immune system is able to eradicate developing tumours.  However some tumours are able to escape elimination and go onto equilibrium (cancer persistence) EQUILIBRIUM (cancer persistence) When incomplete removal is present, tumour cells remain dormant and enter equilibrium. The immune system exerts a potent and relentless pressure that contains the tumour. During this phase, some of the tumour may mutate or give rise to genetic variants that survive, grow and enter the next phase ESCAPE (cancer progression) The expanding tumour populations becomes clinically detectable.
81
describe the mutational (genotoxic) model of cancer
Carcinogens can directly alter the structure of DNA (genotoxic), if this change in DNA is not repaired then it leads to an increased chance in developing a tumour. The presence of multiple mutations in critical genes in a distinctive feature of cancer cells and supports that cancer arises through the accumulation of irreversible DNA damage

CELLULAR PATHOLOGY (10 decks)

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